“Our study demonstrates the high sensitivity of [gallium Ga-68 dotatate] in the localization of [ectopic Cushing’s syndrome], for both occult primary tumors and metastatic lesions,” the researchers wrote. “Importantly, the use of [gallium Ga-68 dotatate] impacted clinical management in 64% of patients with [ectopic Cushing’s syndrome] overall.” The researche […]

The 11th annual Pituitary Day will take place on October 19, 2019 Patients living with pituitary disorders can hear lectures from our pituitary specialists, see movies of pituitary surgeries and hear from other patients about their experience living with pituitary disease and undergoing surgery.

Cynthia is from Ruckersville, VA. She is testing for Cushing's due to many symptoms. tested for CD because after exhaustive research on AVN (Avascular Necrosis) related to other diseases. I have four known areas of AVN & after seeing the symptoms of CD, I realized may have this. I also have numerous other diseases Lupus, Sojgrens, Hypothyroid, High […]

Today is the Thirteenth Anniversary of my kidney cancer surgery. These thirteen years have been bonus years for me. For my cancer stage, the 5-year survival rate was 81% and I’ve made it more than twice that long – so far.

Kathy was diagnosed with a pituitary tumor in 1991. At the time the only symptom she was aware of was a severe headache. She had a transsphenoidal resection followed by radiation therapy for 23 days. They said they could not remove all of the tumor.

Sadly, we lost another Cushing’s patient on Friday, May 9, 2014. Melinda was a member of the Cushing’s Help message boards since Jun 24, 2007. She was only 25 and left behind a young son and many loving family members.

He died of a presumed heart attack. September 19, 2015 he said "'I was diagnosed hypertensive way back when I was 20. The condition remained for years, and became more acute with my cushings pit tumor. I still have high blood pressure, partially teated with three meds. I'll have to consult my doc and see if this may also be an issue."

'My name is Caroline and I dont post often but have met a few of you guys and read the board regularly, it has definitely been a godsend to cushies everywhere. The reason I am writing tonight is I have just received devastating information about a dear friend of mine, and a woman some of you may have met during testing. Her name is Kathryn Miller and sh […]

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Patients with subclinical hypercortisolism, i.e., without symptoms of cortisol overproduction, and adrenal incidentalomas recover their hypothalamic-pituitary-adrenal (HPA) axis function after surgery faster than those with Cushing’s syndrome (CS), according to a study.

Moreover, the researchers found that an HPA function analysis conducted immediately after the surgical removal of adrenal incidentalomas — adrenal tumors discovered by chance in imaging tests — could identify patients in need of glucocorticoid replacement before discharge.

Using this approach, they found that most subclinical patients did not require treatment with hydrocortisone, a glucocorticoid taken to compensate for low levels of cortisol in the body, after surgery.

The HPA axis is the body’s central stress response system. The hypothalamus releases corticotropin-releasing hormone (CRH) that acts on the pituitary gland to release adrenocorticotropic hormone (ACTH), leading the adrenal gland to produce cortisol.

As the body’s defense mechanism to avoid excessive cortisol secretion, high cortisol levels alert the hypothalamus to stop producing CRH and the pituitary gland to stop making ACTH.

Therefore, in diseases associated with chronically elevated cortisol levels, such as Cushing’s syndrome and adrenal incidentalomas, there’s suppression of the HPA axis.

After an adrenalectomy, which is the surgical removal of one or both adrenal glands, patients often have low cortisol levels (hypocortisolism) and require glucocorticoid replacement therapy.

“Most studies addressing the peri-operative management of patients with adrenal hypercortisolism have reported that irrespective of how mild the hypercortisolism was, such patients were given glucocorticoids before, during and after adrenalectomy,” the researchers wrote.

Evidence also shows that, after surgery, glucocorticoid therapy is administered for months before attempting to test for recovery of HPA function.

For the past 30 years, researchers at the University Hospitals Cleveland Medical Center have withheld glucocorticoid therapy in the postoperative management of patients with ACTH-secreting pituitary adenomas until there’s proof of hypocortisolism.

“The approach offered us the opportunity to examine peri-operative hormonal alterations and demonstrate their importance in predicting need for replacement therapy, as well as future recurrences,” they said.

In this prospective observational study, the investigators extended their approach to patients with subclinical hypercortisolism.

“The primary goal of the study was to examine rapid alteration in HPA function in patients with presumably suppressed axis and appreciate the modulating impact of surgical stress in that setting,” they wrote. Collected data was used to decide whether to start glucocorticoid therapy.

The analysis included 14 patients with Cushing’s syndrome and 19 individuals with subclinical hypercortisolism and an adrenal incidentaloma. All participants had undergone surgical removal of a cortisol-secreting adrenal tumor.

“None of the patients received exogenous glucocorticoids during the year preceding their evaluation nor were they taking medications or had other illnesses that could inﬂuence HPA function or serum cortisol measurements,” the researchers noted.

Glucocorticoid therapy was not administered before or during surgery.

To evaluate HPA function, the clinical team took blood samples before and at one, two, four, six, and eight hours after the adrenalectomy to determine levels of plasma ACTH, serum cortisol, and dehydroepiandrosterone sulfate (DHEA-S) — a hormone produced by the adrenal glands.

Pre-surgery assessment of both groups showed that patients with an incidentaloma plus subclinical hypercortisolism had larger adrenal masses, higher ACTH, and DHEA-S levels, but less serum cortisol after adrenal function suppression testing with dexamethasone.

Dexamethasone is a man-made version of cortisol that, in a normal setting, makes the body produce less cortisol. But in patients with a suppressed HPA axis, cortisol levels remain high.

After the adrenalectomy, the ACTH concentrations in both groups of patients increased. This was found to be negatively correlated with pre-operative dexamethasone-suppressed cortisol levels.

Investigators reported that “serum DHEA-S levels in patients with Cushing’s syndrome declined further after adrenalectomy and were undetectable by the 8th postoperative hour,” while incidentaloma patients’ DHEA-S concentrations remained unchanged for the eight-hour postoperative period.

Eight hours after surgery, all Cushing’s syndrome patients had serum cortisol levels of less than 2 ug/dL, indicating suppressed HPA function. As a result, all of these patients required glucocorticoid therapy for several months to make up for HPA axis suppression.

“The decline in serum cortisol levels was slower and less steep [in the incidentaloma group] when compared to that observed in patients with Cushing’s syndrome. At the 6th–8th postoperative hours only 5/19 patients [26%] with subclinical hypercortisolism had serum cortisol levels at ≤3ug/dL and these 5 were started on hydrocortisone therapy,” the researchers wrote.

Replacement therapy in the subclinical hypercortisolism group was continued for up to four weeks.

Results suggest that patients with an incidentaloma plus subclinical hypercortisolism did not have an entirely suppressed HPA axis, as they were able to recover its function much faster than the CS group after surgical stress.

Women with overweight and class I obesity appear to have the lowest cortisol levels, while more significant obesity appears to be associated with higher cortisol levels, according to recent findings.

In the cross-sectional study, Karen K. Miller, MD, of Massachusetts General Hospital, and colleagues evaluated 60 premenopausal women aged 18 to 45 years: 28 with overweight or obesity, 18 with anorexia nervosa and 21 healthy controls at normal weight. Overweight was defined as BMI 25 to 29.9 kg/m2, and obesity was classified as class I (30-34.9 kg/m2) and class II (35-39 kg/m2).

Anorexia nervosa was classified based on DSM-IV criteria, which includes extreme fear of weight gain, body image dysmorphia, weight that is 85% of ideal body weight and cessation of menstruation for 3 consecutive months. Participants were asked to collect 24-hour urine samples, in addition to 11 p.m. and 7 a.m. salivary samples within 1 week of an inpatient hospital visit. For each sample, researchers assessed creatinine clearance, and urinary free cortisol/creatinine clearance was calculated for each specimen to account for the decreased creatinine and filtered cortisol linked to anorexia nervosa.

During the inpatient visit, participants underwent placement of an IV catheter and fasting blood was sampled every 20 minutes from 8 p.m. to 8 a.m. Fasting cortisol and cortisol binding globulin concentrations were measured at 8 a.m. Participants were asked to take 5 g of oral dexamethasone every 6 hours for 48 hours to decrease endogenous disparities in cortisol levels.

The researchers found that with the exception of dexamethasone-suppression-CRH testing, all cortisol measures exhibited a U-shaped association with BMI, most notably urinary free cortisol/creatinine clearance (P = .0004) and mean overnight serum cortisol (P < .0001).

The lowest cortisol levels were seen in the overweight-class I obesity range, and these were also associated with visceral fat tissue and total fat mass. Participants with anorexia nervosa had higher mean cortisol levels than participants with overweight or obesity. Attenuated inverse relationships were seen between lean mass and some measures of cortisol, and most measures of cortisol were inversely related to posterior-anterior spine and total hip bone mineral density.

According to the researchers, these findings have not determined the precise nature of the relationship between cortisolemia, hypothalamic-pituitary-adrenal activation and adiposity.

“The [hypothalamic-pituitary-adrenal] axis activation associated with obesity and excess adiposity raises the question of whether hypercortisolemia contributes to increased adiposity in the setting of caloric excess, whether increased adiposity drives [hypothalamic-pituitary adrenal] activation, or whether the relationship between hypercortisolemia and adiposity is bidirectional,” the researchers wrote. – by Jennifer Byrne